Brain Advance Access originally published online on June 4, 2003
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Brain, Vol. 126, No. 8, 1883-1894,
August 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg183
Short and long latency afferent inhibition in Parkinson’s disease
1 Division of Neurology and Krembil Neuroscience Centre, Toronto Western Research Institute, University Health Network, University of Toronto, Ontario, Canada and 2 Department of Neurology, University of Tübingen, Germany
Correspondence to: Dr Robert Chen, 5W445, Toronto Western Hospital, 399 Bathurst Street Toronto, Ontario, Canada M5T 2S8 E-mail: robert.chen{at}uhn.on.ca
Sensory abnormalities have been reported in Parkinson’s disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of 
20 ms, and long latency afferent inhibition (LAI) at an ISI of 200 ms. We studied SAI and LAI in 10 Parkinson’s disease patients with the aim of assessing whether sensorimotor processing is altered in Parkinson’s disease. Patients were studied on and off medication, and the findings were compared with 10 age-matched controls. Median nerve and middle finger stimulation were delivered 20–600 ms before TMS to the contralateral motor cortex. The motor evoked potentials were recorded from the relaxed first dorsal interosseous (FDI) muscle. SAI was normal in Parkinson’s disease patients off dopaminergic medications, but it was reduced on the more affected side in Parkinson’s disease patients on medication. LAI was reduced in Parkinson’s disease patients compared with controls independent of their medication status. LAI reduced long interval intracortical inhibition in normal subjects but not in Parkinson’s disease patients. The different results for SAI and LAI indicate that it is likely that separate mechanisms mediate these two forms of afferent inhibition. SAI probably represents the direct interaction of a sensory signal with the motor cortex. This pathway is unaffected by Parkinson’s disease but is altered by dopaminergic medication in Parkinson’s disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non-dopaminergic manifestation of Parkinson’s disease.
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